Dr Astwood presents a lecture to explain that the causes of obesity were due to hormonal problems instead of "the conviction of the primacy of gluttony" or that obesity was caused by simply eating too many calories.
July 22, 1962
The Heritage of Corpulence
The Heritage of Corpulence
E. B. ASTWOOD, M.D.
OBESITY is a disorder which, like venereal disease, is blamed upon the patient. The finding that treatment doesn’t work is ascribed to lack of fortitude. Corpulence in America is regarded along with narcotic addiction as something wicked, and I shall not be surprised if soon we have a prohibition against it in the name of national security. The condition is referred to in disparaging terms, including the most impolite references to the appetite. Appetite is held to be the cause, but I say it is hunger. I wish to propose that obesity is an inherited disorder and due to a genetically determined defect in an enzyme; in other words, that people who are fat are born fat, and nothing much can be done about it. I would like further to propose that the more serious of the consequences of being fat are not due to the corpulence but to the inherited defects; if this be so and we like food, we might as well eat up and be happy.
Gary Taubes. The Case for Keto: Rethinking Weight Control and the Science and Practice of Low-Carb/High-Fat Eating (Kindle Locations 345-351). Knopf. Kindle Edition.
A brief lesson in the history of obesity research
On June 22, 1962, a Tufts University Medical School professor named Edwin Astwood tried and failed to correct how we think about the cause of obesity. We have been living with that failure ever since. Astwood was presenting a counterargument to what had become since the end of the Second World War the dominant thinking among medical authorities and researchers on why we get fat. Astwood called this thinking “the conviction of the primacy of gluttony,” by which he meant the unshakable belief that virtually all cases of obesity, child or adult, mild or extreme, are caused ultimately by the overconsumption of calories; that is, people get fat because they eat too much. Astwood considered this belief system—for that’s what it is—to be almost willfully naïve and perhaps the primary reason so little progress had been made in understanding obesity, let alone preventing and treating it. It is also the reason those who have the misfortune to suffer from obesity are held responsible for their condition. “Obesity is a disorder,” he said in opening his presentation, “which, like venereal disease, is blamed upon the patient,” the direct consequence of their failing. Astwood was an endocrinologist; his medical expertise and the subject of his research were hormones and hormone-related disorders. The venue for his talk was the forty-fourth annual meeting of the Endocrine Society. Astwood was its president that year, and his talk, titled “The Heritage of Corpulence,” was his presidential address. Astwood was also a member of the prestigious National Academy of Sciences. According to his NAS biographical essay, his peers considered him “a brilliant scientist” who had contributed more to our understanding of thyroid hormones and how they work than anyone alive. (He won the Lasker Award, considered one step below the Nobel Prize, for the thyroid work.) Of the young men and women who learned to do their medical research in Astwood’s Boston-area laboratory, thirty-five would go on to become full professors by the time Astwood passed away in 1976. He was “not only driven by an insatiable curiosity,” the NAS biography says of Astwood, “but by a curiosity that sought answers with willful determination.” Although Astwood was known among his friends and colleagues for having little interest in food or eating—he considered meals only “a necessary intervention in the day’s activities solely for the purpose of bodily nutrition”—much of his laboratory work in the latter years of his research career was dedicated to understanding obesity, specifically the influence of hormones on fat accumulation and the use of fat to fuel our metabolism. In the small world of 1960s-era obesity research, Astwood was something of a throwback to the pre–World War II years. While he had a profound understanding of the research literature on obesity and was a serious if not indeed brilliant scientist, he had been a physician also who treated patients in his clinic. In this he was like the physician researchers in Germany and Austria before the war who had dominated thinking on obesity and had also come to their conclusions on the nature of the obese condition by observing it closely in their human patients, taking their histories and coming to understand what they were going through and living with. Doctors would do that with any other disorder—why not do it with such a seemingly intractable disorder as obesity? Many of the most influential of those prewar European authorities had become convinced that obesity must be the result of a hormonal or metabolic dysfunction, not caused by overeating, a concept that they recognized as circular logic. (“To attribute obesity to ‘overeating,’ ” the Harvard nutritionist Jean Mayer had aptly commented eight years before Astwood’s presentation, “is as meaningful as to account for alcoholism by ascribing it to ‘overdrinking.’ ” It’s saying the same thing in two different ways, at best describing the process, not explaining why it’s happening.) Rather, it’s somehow programmed into the very biology of the fat person, a disorder of fat accumulation and fat metabolism, these German and Austrian clinical researchers concluded. They believed, as Astwood came to believe, that obesity is neither a behavioral issue nor an eating disorder, not the result of how much we choose to eat consciously or unconsciously. That German-Austrian research community had evaporated, beginning in 1933 with the rise of the Nazi Party. By the time the war was over, European thinking on obesity, grounded in decades of clinical experience and observation, had evaporated with it. The very lingua franca of medicine shifted from German prewar to English postwar. German-language medical literature was considered of little interest, even unreadable by the new generation of young American physicians and nutritionists, who repopulated the field and found the conventional, simplistic thinking on obesity all too easy to believe. With just a few exceptions, these newly minted experts weren’t burdened with actually having to help obese patients achieve a relatively healthy weight for life. They were guided instead by a theory—technically, a hypothesis—that they believed in unconditionally. They believed the truth was obvious, which is always an impediment to making progress in any scientific endeavor. Their truth was the subject of Astwood’s presentation: a “conviction in the primacy of gluttony,” the notion that obesity is almost invariably caused by eating too much, consuming more calories than we expend, and so is ultimately a behavioral or eating disorder. That conviction implied that the only meaningful difference between lean people and people who struggled with obesity is that the lean can control their food intake and hence their appetites—consume only as many calories as they expend—while people with obesity could not, or at least not once they started to get fat. The idea that the fat tissue of those who become obese might have some physiological drive to accumulate fat that the tissues of lean people don’t, some subtle hormonal disruption, was dismissed by the authorities as nothing more than “lame excuses” (quoting the Mayo Clinic’s leading 1960s-era obesity expert) for fat people not to do what came naturally to lean people—eat in moderation. If anything, the supposedly learned postwar authorities came to consider obesity the result of a psychological defect, not a physiological one. They were not shy in stating that people got fat primarily because of “unresolved emotional conflicts” or because they had “turned toward food to relieve some of the nervous tensions of life.” These authorities counseled those with obesity to embrace a lifetime of walking away from their meals still hungry, of semistarvating themselves, ideally after consulting a psychiatrist first. This is the thinking that Astwood hoped to overturn with his presidential address. He enumerated with elegance and occasional humor the reasons why obesity was surely a genetic disorder, which implied that it almost assuredly had to be a hormonal or endocrinological one. Yes, he acknowledged, this was the implication every time someone afflicted with obesity made a comment along the lines of “everything I eat turns to fat.” It was anything but a lame excuse, according to Astwood; it was a reality. It was true, he said, not just for the kind of extreme obesity that he occasionally saw in patients in his practice, but for “the common or garden varieties … the kind that we see every day.” One thing that seemed to mystify Astwood was that there was nothing subtle about the evidence arguing for a genetic, and so hormonal, influence in obesity and fat accumulation. Obesity ran in families, Astwood said, as the authorities all agreed, but not because fat parents overfed their children. It did so because of a strong genetic component. Identical twins don’t just have the same faces; they have identical body types. If one twin is obese, so almost assuredly will the other one be. Even the distribution of obesity in families suggested genetics were involved. Astwood told his audience about one of his patients who was twenty-four years old, five feet four inches tall, and weighed 457 pounds. This young man had seven siblings, three of whom also suffered from extreme obesity: “His brothers, aged 10, 15, and 21, weighed respectively 275, 380, and 340 pounds.” The four other siblings “were of normal proportions.”
This “looked more like the work of genes,” said Astwood, not the “product of a groaning family board,” an antiquated phrase that refers to a dining table overloaded with food. We know that genes determine stature and hair color, said Astwood, and they determine the size of our feet and a “growing list of metabolic derangements, so why can’t heredity be credited with determining one’s shape?” If we had doubts that this was the case, we only had to look at animals. “Consider the pig,” he said: “His corpulence and gluttony resulted from man’s artificial selection; selective breeding provided us with this hulk with his hoggish ways, and no one will convince me that his gourmandizing is provoked by parental oversolicitude.” A reasonable picture of how those genes might be expressing themselves, Astwood explained, had been worked out since the 1930s. A series of laboratory researchers had generated an enormous amount of information about how our bodies regulate the fat we store and the fat we use for energy. “To turn what is eaten into fat, to move it and to burn it requires dozens of enzymes and the processes are strongly influenced by a variety of hormones,” he explained. Sex hormones clearly play a role in where fat is stored. Men and women, after all, tend to fatten differently: men above the waist, women below it. Thyroid hormones, adrenaline, and growth hormones all play a role in releasing fat from its depots, as does a hormone known as glucagon, secreted by the pancreas. “The reverse process,” Astwood said, “reincorporation of fat into the depots and the conversion of other food to fat, tends to be reduced by these hormones, but to be strongly promoted by insulin.” All this demonstrated “what a complex role the endocrine system plays in the regulation of fat.” An important clue to what might be happening, he added, is the fact that the numerous chronic disorders associated with obesity—“particularly those involving the arteries”—resemble arteries”—resemble those that come with diabetes so closely, it implies “a common defect in the two conditions.” Now imagine, Astwood suggested to his audience, what would happen if just one of these mechanisms went awry, impeding the release of fat from fat cells or promoting its storage. It was all too easy to imagine a slow, gradual accumulation of fat that could lead to extreme obesity if continued over years and decades. As the fat inexorably accumulated, a likely result would be what Astwood described as “internal starvation,” as the body hoarded calories in fat cells that it would otherwise need for fuel, while simultaneously increasing the weight that had to be carried around, day in and day out, requiring the expenditure of more and more energy to move and fuel that bulk. In other words, the same subtle hormonal disruption that could cause fat to accumulate to excess would also make a fat person hungry while it was happening. This would be exacerbated by the advice given to the fat person
from all sides: Eat less, exercise more. Starve yourself, if necessary. If the proposed treatment for a fat accumulation problem that itself caused internal starvation—that is, hunger—was to starve even more, we can imagine all too easily why it would fail, if not in the short run, certainly eventually. “This theory,” Astwood said, “would explain why dieting is so seldom effective and why most fat people are miserable when they fast. It would also take care of our friends, the psychiatrists, who find all kinds of preoccupation with food, which pervades dreams among patients who are obese. Which of us would not be preoccupied with thoughts of food if we were suffering from internal starvation? Add to the physical discomfort the emotional stresses of being fat, the taunts and teasing from the thin, the constant criticism, the accusations of gluttony and lack of ‘will power,’ and the constant guilt feelings, and we have reasons enough for the emotional disturbances which preoccupy the psychiatrists.”